(BSc Universit茅 de Montr茅al, PhD 平特五不中)
Associate Member
Lyman Duff Medical Building
3775 University St., Room 610
Tel: (514) 398-5592
Fax: (514) 398-7052
[ MailTo('Email', 'martin.olivier [at] mcgill.ca', 0); ]
Leishmania
In the last 10 years, we found that macrophage signaling pathways alteration (eg JAK2/STAT1alpha) upon Leishmania infection were responsible for their functional inhibition. Recently we reported that this parasite could activate negative regulatory mechanisms of the host, such as the protein tyrosine phosphatase SHP-1, to fulfill some of these inhibitions. Our research program is dedicated to discover the cellular and molecular mechanisms regulating these inactivation processes.
Plasmodium and Malaria
Hemozoin (HZ) is an inert molecule resulting from heme polymerization and released by Plasmodium-infected red blood cells during malaria. Once in circulation HZ is avidly engulfed by phagocyte, and it is proposed that modulation of macrophage functions by this crystalline molecule is responsible for the development of malaria pathologies. We recently reported that Plasmodium falciparum HZ and its synthetic counterpart were enhancing IFN-gama-induced NO generation by phagocytes. We also showed that HZ was per se a strong inducers of inflammation, conducting to cellular recruitment, and in vivo production of important pro-inflammatory molecules regulated by oxidative stress-dependent and 鈥搃ndependent mechanisms. These findings support the idea that HZ could play an important role in the development of inflammation-mediated pathologies during malaria, and lead us to ask whether HZ is really a key modulator of the innate immune response leading to detrimental condition for the host.
Tel.: 514-398-5592
[ MailTo('Email', 'martin.olivier [at] mcgill.ca', 0); ]
